Journal: Nature communications

Article Title: ARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network.

doi: 10.1038/s41467-024-54410-y

Figure Lengend Snippet: Fig. 3 | Association of ARMH3 with the Golgi complex is dependent on ARL5 and its upstream activators ARFRP1 and SYS1. a Confocal fluorescence micro- scopy of GFP-ARMH3 expressed by transient transfection in the indicated WT and KO HeLa cell lines. GFP-ARMH3 is shown in grayscale and nuclei (DAPI) in blue. Each pair of images shows a lower magnification of a larger field and a higher magnifi- cation of the boxed area. Scale bars: 10 μm. Notice the dissociation of GFP-ARMH3 from the Golgi complex in cells with KO of ARL5, ARFRP1, or SYS1. b Quantification of the percentage of cells with GFP-ARMH3 at the Golgi complex from experiments such as that shown in panel a. Values are the mean ± SD from four independent, color-coded experiments. The statistical significance of the differences was

Article Snippet: A PCR ampliconof human ARMH3 was amplified from HeLa cDNA and subcloned into pmEGFP-1 vector (Addgene, #36409, submitted by Benjamin Glick, University of Chicago) and pcDNA3.1-MTS-BioID2, both of whichwere digestedwith EcoRI-BamHI.

Techniques: Transfection

Journal:

Article Title: Thrombolysis: newer thrombolytic agents and their role in clinical medicine

doi:

Figure Lengend Snippet: Reteplase.

Article Snippet: In the abscence of fibrin, reteplase and alteplase do not differ with respect to their activity as plasminogen activators, nor do they differ with respect to their inhibition by the plasminogen activator inhibitor type 1 (PAI-1). fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 1 caption a7 Alteplase. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 2 caption a7 Reteplase. table ft1 table-wrap mode="anchored" t5 Table 1 caption a7 Component Function Fibronectin finger Binding to fibrin Epidermal growth factor domain Elimination by hepatocytes Kringle 1 Elimination by liver endothelial cells Kringle 2 Stimulation of protease by fibrin Protease domain Splitting of plasminogen Inhibition by PAI-1 Carbohydrate side chain Elimination from plasma Open in a separate window Reteplase, tenecteplase, and lanoteplase are derivatives of alteplase, components of which have been deleted or changed.

Techniques: